Heart disease is the most common chronic disease in the developed world, and quickly increasing the developing world. It is responsible of 16% of the deaths in high income countries and 14% in middle income countries as defined by the World Health Organization. Ischemic heart disease is the most common for mortality, with valvular disease in the second place. Between 2% and 4% of the population over 65 is estimated to have some type of valvular disease. The most common valvular disease is the aortic stenosis, followed by mitral stenosis and mitral regurgitation. Another condition that is not uncommon is subvalvular stenosis due to hypertrophy of the septum (106), where there is an obstruction below the aortic valve that affect the heart in the same way as the aortic stenosis does (FIGS. 1a and b). Subvalvular stenosis increases the work needed for the heart to maintain the blood pressure and cardiac output. When severe, the condition decreases cardiac output with decreased physical strength as a consequence. In addition, the condition increases the likelihood of dying prematurely in heart failure.
Septal hypertrophy is the medical term used when the septum dividing the right and left ventricle of the heart is hypertrophic, i.e. thicker than normally. This thickening will lead to an obstruction in the outflow of the left ventricle. The pathogenesis of septal hypertrophy is mainly twofold. First it could be a part of a hypertrophic cardiomyopathy, where the entire muscle mass of the heart is increased. The second cause is secondary to an aortic stenosis, where the stenosis of the valve leads to an increase in work load and increase in the muscle mass of the septum. In both these conditions, the thickness of the septum (106) increases from a normal 6-10 mm to up to 25-30 mm. The thickest part is just below in the aortic valve in the tubular part of the left ventricle (103) called the outflow tract (104) (FIG. 1b). As the septum (106) bulges into this tubular part, an obstruction will develop in the part where the blood normally is ejected to the circulation.
Currently, the treatment modalities available for septal hypertrophy are 1) surgical myectomi, 2) Alcohol Septal Ablataion (ASA) and 3) dual chamber pace-maker pacing.
Surgical myectomi is done by routine open heart surgery, where the chest is opened by a median sternotomy, the patient is put on heart-lung machine and the heart is arrested. When cardiopulmonary bypass is instituted, the surgeon can open the heart and resect a part of the hypertrophic septum. Alcohol septal ablation is performed by instilling alcohol in the coronary arteries that supplies the septum with blood. The procedure is performed in a catheter lab with the patient awake, and through routine access in the groin. The alcohol will trigger a cell death and necrosis, and thereby decreasing the volume of the septum. Pace-maker therapy is performed to achieve a contraction pattern of the septum that will decrease the outflow obstruction.
All of the above treatment modalities are associated with inconveniences. Surgical myectomi is invasive and can be considered a relatively complicated surgical process involving substantial risks for the patent undergoing the surgery since the chest has to be opened and the heart arrested. ASA and pace-maker therapy can be considered to be selective alternatives for certain cases of e.g. lighter forms of septal hypertrophy in cases where surgical myectomi is not suitable for the patient. The above described techniques for treating septal hypertrophy both have the same disadvantage in that it is difficult to control the amount of septum to remove. Surgical resection depends on the experience of the surgeon to remove the right amount of tissue. If the surgeon removes too much tissue there will be a defect in the septum, in if the surgeon removes too little the patient will not be entirely cured. For ASA the achieved effect is difficult to control as the operator does not know how much of the septum that will go into necrosis.